ERBB signaling in CTCs of ovarian cancer and glioblastoma.

ERBB signaling in CTCs of ovarian cancer and glioblastoma.
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DOI:
10.18632/genesandcancer.162
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发表时间:
2017-11
期刊:
影响因子:
--
通讯作者:
Chaluvally-Raghavan P
Chaluvally-Raghavan P
中科院分区:
其他
文献类型:
--
作者:
Geethadevi A;Parashar D;Bishop E;Pradeep S;Chaluvally-Raghavan P

文献摘要

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循环肿瘤细胞(CTCs)是漂浮的细胞群,它们在脱离原发部位后对肿瘤具有抵抗力,并通过循环系统和淋巴系统传播到全身。ctc被认为是转移的种子细胞,因此分离ctc不需要任何侵入性手术。基于卵巢癌和胶质母细胞瘤的性质和位置,ctc和肿瘤细胞的血液扩散在这些癌症中的作用尚不清楚。由于表皮生长因子受体(EGFR/ERBB)家族成员的过度表达和/或突变而导致的失调已被认为是卵巢癌和胶质母细胞瘤的病因和进展的原因之一。然而,ERBB受体在卵巢癌和胶质母细胞瘤CTC形成中的作用尚不明确。本报告强调了ERBB家族受体在卵巢癌和胶质母细胞瘤中抗肿瘤和CTC形成中的作用。最近对CTCs的研究表明,从循环系统中捕获ERBB受体阳性细胞是分离CTCs用于肿瘤细胞基因组和蛋白质组学表征的有效方法。因此,erbb靶向ctc的分离将有助于设计治疗癌症的疗法,确定癌症患者的药物反应和耐药机制。
Circulating Tumor Cells (CTCs) are floating cell populations, which are resistant to anoikis after detachment from the primary sites and travel through the circulatory and lymphatic systems to disseminate throughout the body. CTCs are considered as seed cells for metastasis, and thus isolation of CTCs does not require any invasive procedure. Based on the nature and location of ovarian cancer and glioblastoma, the role of CTCs and hematogenous (carried by blood) spreading of tumor cells in these cancers were not understood well. Dysregulation of epidermal growth factor receptor (EGFR/ERBB) family members due to their overexpression and/or mutation have been known to contribute to the etiology and progression of ovarian cancer and glioblastoma. However, the role of ERBB receptors on CTC formation of ovarian cancer and glioblastoma is not well established. This report highlights the role of ERBB family receptors on resistance to anoikis and CTC formation in ovarian cancer and glioblastoma. Recent research on CTCs demonstrates that capturing ERBB receptor positive cells from circulating system is an efficient approach to isolate CTCs for genomic and proteomic characterization of tumor cells. Therefore, ERBB-targeted isolation of CTCs would help to design therapy to treat cancer, determine drug responses and drug-resistant mechanisms in cancer patients.